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ePoster
ION CHANNEL CONTROL OF VENTRAL RADIAL GLIA FATE SPECIFIES SOMATOSTATIN INTERNEURONS
Kyungmin Kimand 2 co-authors
KIST
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-134
Presentation
Date TBA
Board: PS07-10AM-134
Event Information
Poster Board
PS07-10AM-134
Poster
View posterAbstract
Cortical circuit assembly depends on timely interneuron production, yet how early ventral radial glia (vRG) bias lineage output remains unclear. The neurotransmitter γ-aminobutyric acid (GABA) excites embryonic progenitors via membrane depolarization and Ca²⁺ signals, however, the channels and logic that couple these signals to lineage choice are unknown. Here we show that the Ca²⁺-activated Cl⁻ channel, Anoctamin 1 (ANO1/TMEM16A) promotes vRG output toward somatostatin (SST) interneurons while limiting intermediate progenitors (IPs) in the medial ganglionic eminence. ANO1 marks a Fabp7⁺/Sox2⁺ vRG subpopulation. Ano1 deficiency reduces vRG proliferation and shifts output toward IPs, accompanied by reduced embryonic and early postnatal SST⁺ cells. Slice electrophysiology and Ca²⁺ imaging support a model in which GABAA receptor activation triggers ER-derived Ca²⁺ oscillations that activate ANO1, sustaining elevated vRG membrane potential and, together with Orai1-dependent Ca²⁺ entry, shaping GABA-evoked Ca²⁺ dynamics. These findings identify an ion channel-dependent mechanism that links early GABA signaling to vRG fate bias toward the SST interneuron lineage.
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